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equine muscle

sgusvm

QuestionAnswer
Many muscle diseases have intermittent clinical signs or are triggered by certain environmental stimuli
Observe size, shape, and symmetry of all muscle groups
Are fasciculations present
Note symmetry of gait
Gait abnormalities may result from pain, muscle weakness, stiffness, muscle cramping, spasticity, decreased range of joint motion,dysfunction of motor neurons and ataxia
Palpation of all major muscle groups for evidence of pain, cramping, fibrosis
Muscle percussion may be performed
Running a needle cap or pen over the lumbar and gluteal muscles should elicit a normal extension (swayback) followed by flexion (hogback)
Horses that guard against running a needle cap or pen over the lumbar and gluteal muscles may have pelvic or thoracolumbar muscular pain
Creatine Kinase (CK) Enzyme responsible for breaking down creatine phosphate to creatine and phosphate, releasing energy for muscular contraction
Found predominantly in skeletal and heart muscle CK
Short plasma half-life (2 hours) CK
Remarkable sensitivity as an indicator of muscle injury CK
Serum CK activity increases within hours of insult
Training, transport, and recumbency can cause mild elevations that quickly return CK to normal (< 8,000 IU/L)
Intramuscular injection may elevate CK
With muscle injury CK elevation is typically > 100,000 IU/L
Aspartate Aminotransferase (AST) Previously known as SGOT (serum glutamic-oxaloacetic transaminase)
High activity level in skeletal/cardiac muscle cells, hepatocytes, RBCs AST
Elevations in AST are not specific for muscle injury
Plasma half-life longer than CK 7–10 days AST
AST activity rises more slowly in response to muscle injury than does CK peaks 12-24 hr after insult
Rule(s) of thumb Increased CK and AST reflect recent or active muscle injury
Persistently elevated CK ongoing muscle injury
Elevated AST with decreasing or normal CK resolving myositis
Lactate Dehydrogenase (LDH) Elevations occur because of damage to various organs in body composed of muscle and heart subunits
Not specific for muscle disease LDH
Myoglobin needed for transport of oxygen into and within muscle cells
Urine dipstick positive for blood in the absence of hemolysis or RBCs in urine is hightly suggestive of myoglobinuria
Evaluation of muscle disorders precipitated by exercise may require an exercise challenge test
Evaluation of muscle disorders precipitated by exercise by induce subclinical elevations in serum CK Requires 15 minutes walking/trotting (lunge line/treadmill)
Pre-exercise blood sample followed by second blood sample taken 4–6 hours following exercise
In normal horses, rarely see > 3-fold increase in CK with exercise
Greater than 5-fold increase indicative of rhabdomyolysis
Not recommended for horses with overt signs of rhabdomyolysis evaluation of muscle disorders by exercise
Electromyography Useful to evaluate muscle tone
In electromyography Normal muscle should produce a burst of electrical activity followed by quiescence
Scintigraphy May be useful for diagnosing deep muscle disease not evident by palpation
Ultrasonography Useful for identification of muscle trauma, crepitus, fibrosis, atrophy
Acute injury areas of hypoechogenicity due to loss of normal muscle fiber striation
Tears in muscle fascia may be identified US
Hematomas may be observed US
Hyperechoic regions may indicated increased connective tissue or loss of muscle cell mass US
Gas echoes and mineralization may also be observed US
Muscle Biopsy Typical sites for percutaneous biopsy in cases of generalized muscle disease Semimembranosus, biceps femoris, middle gluteal
Can use specific muscle if it can be isolated muscle biopsy
Care should be taken to inject anesthetic only into subcutaneous tissue and caution used when handling muscle so as to avoid crush of the sample
Rhabdomyolysis A syndrome of muscle cramping that occurs during physical exertion or exercise
Recurrent Exertional Rhabdomyolysis Common in Thoroughbred linebreeding,Autosomal dominant trait
Recurrent exertional rhabdomyolysis Predisposing environmental triggers Gender (67pct females)Temperature,Diet,Excitement,Exercise duration and intensity,Lameness
Clinical signs and laboratory findings of recurrent exertional rhabdomyolysis Mild to moderate signs of muscle cramping of gluteals, semimembranosus, semitendinosis, biceps femoris, & quads
Mild to severe pain,Anxiety, profuse sweating, refusal to move, increased HR & RR,Affected muscles firm and painful on palpation,May have areas of muscle tearing and edema recurrent exertional rhabdomyolysis
Most cases recover in several hours severe cases may be recumbent recurrent exertional rhabdomyolysis
Recurrent exertional rhabdomyolysis CK, AST, LDH, and myoglobin released into circulation
Systemic acidosis and dehydration promote acute tubular necrosis from pigment nephropathy (ARF) recurrent exertional rhabdomyolysis
Recurrent rhabdomyolysis Possible defect in dihydropyridine or ryanodine receptor and affects calcium regulation
Recurrent Exertional rhabdomyolysis Diagnosis Muscle biopsy suggests disease is similar to malignant hyperthermia in pigs,Caffeine or Halothane muscle contracture test,Biopsy from intercostals muscle Not readily available so diagnose based on history, lab findings, and histopath of muscle
Histopath increased number of central nuclei without evidence of PSSM (glycogen PAS staining)
Treatment for rhabdomyolysis Dietary (decrease carbs, increase fat)Add corn oil / rice bran for additional calories,Manage stress (nervous horses),Dantrolene
Decrease the rate of calcium release from the sarcoplasmic reticulum dantrolene
Used for prevention with success – given orally prior to exercise dantrolene
No data on long-term use / efficacy of drug dantrolene
Polysaccharide Storage Myopathy Common in Quarter horses, Paint horses, Drafts, Warmbloods
Repeated bouts of exertional rhabdomyolysis that in some cases may be induced with little exercise PSSM
Most distinctive characteristic is mild to severe accumulation of abnormal polysaccharide within the myoplasm PSSM
clinical signs and Laboratory findings of PSSM Frequent episodes of muscle cramping and rhabdomyolysis
Increased CK, AST, myoglobinuria PSSM
Mild episodes Stiff gait, anxiety, stretching out PSSM
Severe episodes Anxiety, painful behavior, sweating, reluctance to move, recumbency PSSM
Definitive diagnosis of PSSM from muscle biopsy,abnormal PAS staining of glycogen
PSSM horses often have a calm and sedate demeanor
Classic signs include a posture that resembles a urination stance, a tucked-up abdomen, muscle fasciculations and pawing in the stall post-exercise PSSM
PSSM Elevations of muscle enzymes are usually present and may remain elevated for long periods even when rested
Glycogen accumulation due to increased ability to synthesize glycogen PSSM
PSSM horses have enhanced insulin sensitivity, enhanced glucose clearance, and enhanced synthesis of glycogen
Defect related to deficiency of glycogen synthase 1 PSSM
Treatment of PSSM includes decreasing starch,concentrate from diet,> 13pct fat in digestible energy requirements,Use fat supplementation to provide additional calories,Rice bran,corn oil,alfalfa pellets,Gradual training program to reduce risk of triggering episode
Nutritional Rhabdomyolysis White Muscle Disease Peracute to subacute myodegenerative disease of cardiac and skeletal muscle caused by a dietary deficiency of selenium or vitamin E
one distinct form of white muscle disease Cardiac has sudden onset,severe debilitation,may be found dead,Lesions in heart,diaphragm,intercostal muscles
Skeletal form of nutritional rhabdomyolysis has a slower onset characterized by muscular weakness or stiffness, recumbency possible
Muscles of tongue may be involved, leads to dysphagia skeletal form
Intercostal muscle involvement may lead to respiratory distress skeletal form
Cardiomyopathy may be present,Elevated CK, AST during acute phase,Myoglobinuria white muscle disease
Diagnosis of white muscle disease Measure selenium,Vitamin E,Tissue,whole blood,Measure GSH-Px
Se-dependent glutathione peroxidase Formed in RBCs
Selenium deficient soil in areas across the United States, may predispose
Poor quality hay/lack of green forage leads to Vitamin E deficiency
Necropsy findings Bilaterally symmetrical myodegeneration,Pale discoloration,White streaks in muscle bundles Represent coagulative necrosis,Calcification,intramuscular edema
Cardiac form poor prognosis
Usually not compatible with life cardiac form
Skeletal muscle form may be treatable
Prognosis remains guarded skeletal muscle form
Selenium,Vitamin E supplementation,Injectable selenium/Vit E compounds critical
Additional oral α-tocopherol (Vit E) recommended
Prevention of nutritional rhabdomyolysis white muscle disease supplement mares during gestation,allow access to green forage
Inflammatory Rhabdomyolysis,Clostridial Myonecrosis Infections are characterized by a rapid clinical course, fever, systemic toxemia, and high mortality
Development following IM injection or deep penetrating wound may be the result of direct spore deposition into the tissue inflammatory rhabdomyolysis,clostridial myonecrosis
The spores undergo a conversion into the vegetative, toxin-producing form of the organism
Also, can gain access to the body through the alimentary tract and are present in liver and muscle in the dormant spore form
Proliferation of clostridial agents in devitalized tissues is associated with the release of powerful exotoxins, responsible for the local necrotizing myositis and systemic toxemia Lecithinase and hemolysin
Aggressive treatment with high dose penicillin and muscle fasciotomy inflammatory rhabdomyolysis clostridial myonecrosis
Poor to guarded prognosis for life,very high mortality IRCM
No equine vaccine preventative IRCM
Use good IM injection technique to prevent IRCM
Use muscle groups with effective drainage for injection to prevent IRCM
Monitor IM injection sites CAREFULLY – good client education is a must IRCM
Specific Disorders of Muscle Tone,Hyperkalemic Periodic Paralysis Inherited autosomal dominant trait commonly seen in Quarter Horse, Paints, and Appaloosas
All related to QH stallion Impressive HYPP
Horses may be carriers (heterozygous) and be asymptomatic or be affected with varying degrees of severity HYPP
Homozygous individuals have clinical signs of HyPP
HYPP is due to a point mutation causing a phenylalanine to leucine substitution in a key part of the skeletal muscle sodium channel
This voltage-dependent channel permits rapid membrane depolarization during the initial phase of the action potential skeletal muscle channel
In horses with HYPP, the resting membrane potential is closer to threshold than normal horses
The resting membrane potential is closer to threshold and results in an excessive inward flux of sodium and outward flux of potassium, resulting in persistent depolarization of muscle cells
Clinically, this myopathy manifests as abnormal skeletal muscle membrane excitability leading to episodes of myotonia, sustained muscle contraction and/or paralysis HYPP
During episodes in HYPP serum potassium is generally elevated
Sweating and muscle fasciculations in flank, neck and shoulders may be seen in episodes of HYPP
Stimulation and attempts to move may exacerbate muscular fasciculations during episodes of HYPP
Muscular weakness during HYPP episodes is very common
Respiratory distress from paralysis of muscles of URT / larynx occurs during HYPP episodes
Tracheostomy may be required in some HYPP individuals
HYPP Definitive test is the demonstration of the base-pair sequence substitution in the abnormal segment of the DNA encoding for the alpha subunit of the sodium channel
HYPP Submission samples include hair roots or whole blood in EDTA tubes
EMG may reveal abnormal fibrillation potentials, complex repetitive discharges with occasional myotonic potentials, and trains of doublets even between episodes HYPP
Oral potassium chloride challenge test frequently produces clinical signs within 1-4 hours, but is not recommended
Treatment for HYPP Mild cases may respond with mild exercise (hand-walking) which stimulates epinephrine, which stimulates sodium-potassium ATPase activity to mobilize potassium (drive it intracellularly)
Feeding grain or corn (KARO) syrup to stimulate insulin-mediated movement of potassium across cell membranes may also be helpful treating HYPP
Why should you Avoid molasses in HYPP cases high K+ level
IV dextrose +/- bicarbonate can be used to enhance intracellular movement of potassium
Control HYPP by Decrease dietary potassium and increase renal urinary excretion of potassium
Avoid alfalfa, molasses, canola and soybean oil to help control HYPP
Feed several times a day and Regular exercise In HYPP horses
Acetazolamide (K+ wasting diuretic) causes increased renal potassium ATPase activity and has been shown to stabilize blood glucose and potassium by stimulating insulin secretion
Specific Disorders of Muscle Cramping Synchronous Diaphragmatic Flutter Also known as thumps
Typically occurs in horses suffering from fluid and electrolyte imbalances thumps
Contraction or twitch in the flank region in synchrony with the heart SDF or thumps
Most consistent metabolic derangement reported in horses is low serum ionized calcium associated with hypochloremic metabolic alkalosis
Metabolic alkalosis may alter the ratio of free to bound calcium (increasing calcium binding to protein and decreasing ionized calcium)
Occurs in association with atrial depolarization in horses SDF or thumps
May disrupt the normal membrane potential of the phrenic nerve, which passes directly over the atrium, resulting in nerve discharges in response to atrial depolarization SDF thumps
Created by: alljacks